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Original Research: Critical Care |

The Use of Bioreactance and Carotid Doppler to Determine Volume Responsiveness and Blood Flow Redistribution Following Passive Leg Raising in Hemodynamically Unstable PatientsBioreactance and Carotid Doppler FREE TO VIEW

Paul E. Marik, MD; Alex Levitov, MD, RDCS, FCCP; Alisha Young, MD; Lois Andrews, RN-BC, MSN, CCRN, ACNS-BC
Author and Funding Information

From the Division of Pulmonary and Critical Care Medicine (Drs Marik, Levitov, and Young), Division of Critical Care Ultrasonography, Eastern Virginia Medical School; and Division of Critical Care Nursing (Ms Andrews), Sentara Norfolk General Hospital, Norfolk, VA.

Correspondence to: Paul E. Marik, MD, Eastern Virginia Medical School, 825 Fairfax Ave, Ste 410, Norfolk, VA 23507; e-mail: marikpe@evms.edu


Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2013;143(2):364-370. doi:10.1378/chest.12-1274
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Background:  The clinical assessment of intravascular volume status and volume responsiveness is one of the most difficult tasks in critical care medicine. Furthermore, accumulating evidence suggests that both inadequate and overzealous fluid resuscitation are associated with poor outcomes. The objective of this study was to determine the predictive value of passive leg raising (PLR)-induced changes in stroke volume index (SVI) as assessed by bioreactance in predicting volume responsiveness in a heterogenous group of patients in the ICU. A secondary end point was to evaluate the change in carotid Doppler flow following the PLR maneuver.

Methods:  During an 8-month period, we collected clinical, hemodynamic, and carotid Doppler data on hemodynamically unstable patients in the ICU who underwent a PLR maneuver as part of our resuscitation protocol. A patient whose SVI increased by > 10% following a fluid challenge was considered a fluid responder.

Results:  A complete data set was available for 34 patients. Twenty-two patients (65%) had severe sepsis/septic shock, whereas 21 (62%) required vasopressor support and 19 (56%) required mechanical ventilation. Eighteen patients (53%) were volume responders. The PLR maneuver had a sensitivity of 94% and a specificity of 100% for predicting volume responsiveness (one false negative result). In the 19 patients undergoing mechanical ventilation, the stroke volume variation was 18.0% ± 5.1% in the responders and 14.8% ± 3.4% in the nonresponders (P = .15). Carotid blood flow increased by 79% ± 32% after the PLR in the responders compared with 0.1% ± 14% in the nonresponders (P < .0001). There was a strong correlation between the percent change in SVI by PLR and the concomitant percent change in carotid blood flow (r = 0.59, P = .0003). Using a threshold increase in carotid Doppler flow imaging of 20% for predicting volume responsiveness, there were two false positive results and one false negative result, giving a sensitivity and specificity of 94% and 86%, respectively. We noted a significant increase in the diameter of the common carotid artery in the fluid responders.

Conclusions:  Monitoring the hemodynamic response to a PLR maneuver using bioreactance provides an accurate method of assessing volume responsiveness in critically ill patients. In addition, the study suggests that changes in carotid blood flow following a PLR maneuver may be a useful adjunctive method for determining fluid responsiveness in hemodynamically unstable patients.

Figures in this Article

The cornerstone of treating patients with shock remains as it has for decades: IV fluids. Surprisingly, dosing IV fluid during resuscitation of shock remains largely empirical. Too little fluid may result in tissue hypoperfusion and worsen organ dysfunction; however, overprescription of fluid also appears to impede oxygen delivery and compromises patient outcome. Recent data suggest that early aggressive resuscitation of critically ill patients may limit or reverse tissue hypoxia and progression to organ failure and improve outcome.13 However, overzealous fluid resuscitation has been associated with increased complications, length of ICU and hospital stay, and mortality.47

Fundamentally, the only reason to give a patient a fluid challenge is to increase stroke volume (volume responsiveness). If the fluid challenge does not increase stroke volume, volume loading has no useful benefit and may be harmful to the patient. Clinical studies have consistently demonstrated that only about 50% of hemodynamically unstable patients are volume responsive.8,9 Logic dictates that the first step in the resuscitation of any hemodynamically unstable patient is to determine whether the patient is a volume responder. A number of dynamic techniques based on heart-lung interactions during mechanical ventilation have emerged over the past decade to predict volume responsiveness.10 The most important limitation of these techniques is that they can only be performed in patients undergoing mechanical ventilation and that an arterial catheter usually is required. These limitations preclude the evaluation of most patients in the early golden hours of resuscitation in the ED and ICU.

Lifting the legs passively from the horizontal position induces a gravitational transfer of blood from the lower limbs toward the intrathoracic compartment. This technique, known as passive leg raising (PLR), produces a hemodynamic response similar to that of a 200- to 300-mL fluid bolus.1113 Beyond its ease of use, this method has the advantage of reversing its effects once the legs are tilted down. Therefore, PLR may be considered a reversible autotransfusion. The PLR maneuver coupled with the noninvasive assessment of stroke volume would appear to be the ideal method for determining volume responsiveness. Bioreactance cardiac output measurement is based on an analysis of relative phase shifts of an oscillating current that occurs when the current traverses the thoracic cavity.14 Bioreactance technology provides a validated, real-time, noninvasive, and simple method to dynamically measure changes in stroke volume induced by therapeutic interventions.1419 In our ED and ICU, the change in stroke volume index (SVI) (using bioreactance) following a PLR maneuver and fluid challenge are routinely used to assess volume responsiveness. The bioreactance data are recorded in our electronic medical record (EPIC Hyperspace; Epic Systems Corporation). As part of our routine clinical protocol in hemodynamically unstable patients in the ICU, bedside echocardiography (to determine baseline left ventricular function) and changes in carotid and brachial blood flows are determined. This experience has given us the opportunity to determine the accuracy of the PLR maneuver and the utility of carotid blood flow measurement in assessing fluid responsiveness in hemodynamically unstable patients.

We performed an electronic chart review of adult patients admitted to the general ICU at Sentara Norfolk General Hospital between June 2011 and February 2012. This study was approved by the Eastern Virginia Medical School Institutional Review Board (11-11-WC0259) and that of Sentara Norfolk General Hospital. We queried our electronic medical record and included patients in whom a bioreactance-coupled PLR maneuver had been performed and in whom carotid blood flow data were available. The PLR maneuver was standardized and performed in the following manner13: Once the SVI had stabilized and starting with the patient in a 45° semirecumbent position, the patient was placed in a supine position with the legs elevated to 45° using a foam wedge. The maximal change in SVI within the first 3 min of the patient assuming the supine position was recorded as well as the percentage change in SVI. Simultaneously, baseline and supine carotid and brachial Doppler blood flow studies were obtained as outlined later. (These studies were performed by a single investigator [A. L.] during weekdays.) After the PLR maneuver, the patients were placed back in the 45° semirecumbent position. During the study period, all patients received a 500-mL bolus of normal saline given over 10 min through a pressure bag after the PLR maneuver. A patient whose SVI increased by ≥ 10% following the fluid bolus was considered to be fluid responsive. Patients who were fluid responsive received further fluid boluses until they were no longer fluid responsive. Patients who were not in sinus rhythm were excluded from this study. All patients were receiving pressure-controlled ventilation targeted to keep the plateau pressure at < 30 cm H2O and to achieve a tidal volume of 6 to 8 mL/kg ideal body weight. In those patients undergoing mechanical ventilation, the stroke volume variation (SVV) as measured by the NICOM monitor (Cheetah Medical, Inc) was recorded prior to the PLR maneuver.

Ultrasonographic images were obtained with the patient in a semiupright position and then supine with the legs passively raised at 45° (the PLR maneuver). All the ultrasonic images were obtained by a vascular certified echocardiographer (A. L.). The echocardiographer was blinded to the bioreactance data. The images were acquired with a commercially available ultrasound system (LOGIQ e; GE Healthcare) and a 7- to 12-MHz variable frequency linear array transducer. An image of the common carotid artery (CCA) was obtained in the short-axis view, and the maximal CCA diameter was recorded. The transducer was then rotated 90° into the long axis with attempts made to obtain an image with the same CCA diameter as recorded in the short axis. The position of the transducer was marked, and the same acoustic window was used for repeat images. Intraobserver variability was reduced by obtaining three separate images. The CCA diameter was measured in centimeters from intimal to intimal edge at 90° (perpendicular) to the vessel wall in the long-axis view (Fig 1). The velocity time integral in centimeters was determined automatically through digitalized Doppler spectral envelopes, with the sample obtained in the middle of the artery. The sample gate size was not changed through the duration of the study. Blood flow per minute was determined automatically using the following standard formula: blood flow per minute = π × (CCA diameter)2/4 × velocity time integral × heart rate. The Doppler data were obtained at the same angle before and after the PLR maneuver. A similar methodology was used to measure brachial artery blood flow. We have shown a high degree of reproducibility of this technique (data not shown). A full echocardiographic examination was also performed, and the left ventricular ejection fraction (LVEF) was determined using the Teichholz formula.20

Figure Jump LinkFigure 1. Carotid artery Doppler flow imaging at baseline and after a passive leg raising maneuver in a fluid responder. Carotid blood flow increased by 80%, and the vascular diameter increased by 20%. Note the increase in both systolic and diastolic flow. ED = end-diastolic velocity; PS = peak systolic velocity; TAMAX = time average maximum; TAMEAN = time average mean; VF = volume flow.Grahic Jump Location

The following deidentified patient data were abstracted and recorded in an electronic spreadsheet (Excel 2010; Microsoft Corporation): age and sex, major diagnosis, severe sepsis (yes or no), ventilation (yes or no), bioreactance data (SVI, cardiac output [CO], and CO before and after the PLR and fluid challenge), LVEF, and Doppler data. We recorded data only for the paired PLR and (first) fluid challenge. The SVV was recorded only in those patients undergoing mechanical ventilation (with standard ventilator settings). Because few patients had arterial lines in place at the time of the first fluid challenge, the pulse pressure variation was not recorded. Severe sepsis was defined according to the American College of Chest Physicians/Society of Critical Care Medicine consensus criteria.21 Summary statistics were used to describe the clinical data. A patient whose SVI increased by ≥ 10% following a fluid challenge was considered a true fluid responder; that is, the bioreactance response to a fluid challenge was considered the “gold standard” and used to stratify patients as fluid responders or nonresponders. The sensitivity and specificity of the PLR and carotid Doppler flow imaging techniques for predicting volume responsiveness were determined using this gold standard. Student t test was used to compare data between the true responders and the nonresponders. Linear regression was performed to determine the relationship between the change in SVI following PLR and the change in carotid Doppler flow imaging. Unless otherwise stated, all data are expressed as mean ± SD, with statistical significance declared for P ≤ .05.

During the study period, 49 hemodynamically unstable patients underwent a bioreactance-coupled paired PLR and fluid challenge, 34 of whom had simultaneous measurements of carotid blood flow. A complete data set was available on these 34 patients. Their mean age was 64 ± 10 years; 18 (53%) were men. Twenty-two patients (64.7%) had severe sepsis/septic shock, whereas 21 (62%) required vasopressor support and 19 (56%) required mechanical ventilation. Eighteen patients (53%) had an increased SVI of > 10% after the fluid challenge and were considered true fluid responders. Seventeen patients demonstrated an increase in SVI of > 10% after the PLR maneuver (Table 1). All of these patients were true volume responders. One additional patient whose SVI increased by 5.9% after the PLR maneuver (and carotid flow by 133%) had an increase in SVI of > 10% after the fluid bolus. The PLR maneuver, therefore, had a sensitivity of 94% and a specificity of 100% for predicting volume responsiveness using the bioreactance monitor.

Table Graphic Jump Location
Table 1 —PLR Responder and Nonresponder Characteristics

Data are presented as mean ± SD or counts. CO = cardiac output; PLR = passive leg raising; SVI = stroke volume index.

a 

Bilateral carotid blood flow as percentage of CO.

The LVEF was 60% ± 14% in the responders and 45% ± 16% in the nonresponders (P = .02). There was no correlation between the LVEF and percent change in SVI in the responders (r = 0.04, P = .85). In the 19 patients undergoing mechanical ventilation, the SVV was 18.0% ± 5.1% in the responders and 14.8% ± 3.4% in the nonresponders (P = .15). Carotid blood flow (mL/min) increased by 79% ± 32% after the PLR in the responders compared with 0.1% ± 14% in the nonresponders (P < .001). There was a strong correlation between the percent change in SVI by PLR and the concomitant percent change in carotid blood flow (r = 0.59, P = .0003). Using an increase in carotid blood flow of 20% for predicting volume responsiveness, there were two false positive results and one false negative result, giving a sensitivity and specificity of 94% and 86%, respectively. We noted a significant increase in the diameter of the CCA in the fluid responders (Fig 1, Table 1). Changes in brachial artery blood flow after the PLR maneuver were available in a subset of eight patients (five responders and three nonresponders). The brachial arterial blood flow increased by 12% in the responders compared with 0.2% in the nonresponders (Fig 2).

Figure Jump LinkFigure 2. Brachial artery Doppler flow imaging at baseline and after a passive leg raising maneuver in a fluid responder. Brachial blood flow increased by 7%, and the vascular diameter remained unchanged. Note the absence of diastolic blood flow. See Figure 1 legend for expansion of abbreviations.Grahic Jump Location

In this study, we have demonstrated that the PLR maneuver coupled with bioreactance monitoring is a simple and accurate method for determining volume responsiveness in a heterogenous group of hemodynamically unstable patients. The response to PLR correlated very closely with the simultaneous change in carotid blood flow, and there was very good agreement between the patients who were volume responders following PLR and the fluid bolus. The study supports the findings of Benomar et al22 who used bioreactance monitoring in 75 patients post-cardiac surgery, demonstrating that the change in CO following a fluid bolus was highly correlated with the change in CO following PLR. Because the maximal hemodynamic effects of PLR occur within the first minutes of leg elevation, it is important to assess these effects with a method able to track changes in SVI in real time.11 Both bioreactance and carotid Doppler flow imaging are noninvasive technologies ideally suited for this task. The findings of the present study are further supported by a recent meta-analysis that pooled the results of eight studies and confirmed the excellent value of PLR to predict volume responsiveness in critically ill patients, with a global area under the receiver operating characteristic curve of 0.95.23 It is interesting to note that the responders had a higher LVEF and tended to have a lower initial SVI than the nonresponders, suggesting that these patients had preload reserve (were dry). In the present study, only 53% of patients were fluid responders; this finding has been reported with remarkable consistency in the literature8,9 and emphasizes the need to stratify patients as fluid responders or nonresponders prior to embarking on fluid resuscitation. In the present study, the SVV was poorly predictive of volume responsiveness. This finding is at odds with our prior meta-analysis.10 It should be pointed out, however, that most of the studies included in our meta-analysis were performed under highly controlled conditions in the operating room. The patients in the present study were ventilated with a lung protective ventilatory strategy (6-8 mL/kg ideal body weight). Previous studies have demonstrated that SVV and pulse pressure variation are predictive of fluid responsiveness only in patients ventilated with a tidal volume of ≥ 8 mL/kg ideal body weight.24,25 Furthermore, recent studies indicated that in routine clinical practice, the SVV and other variables that depend on heart-lung interaction during mechanical ventilation may not reliably predict volume responsiveness.26 The advantage of bioreactance is that it is totally noninvasive, does not require endotracheal intubation or an arterial line, and provides a good estimate of stoke volume in patients with atrial fibrillation. During the study period, ongoing fluid resuscitation and fluid responsiveness were based on the response to a fluid challenge. However, following the analysis of these data, we currently resuscitate patients based on the results of a PLR maneuver alone. This approach has the advantage of limiting the amount of fluid given to nonresponders and allows the assessment of volume responsiveness to be determined in < 5 min.

To our knowledge, this study is the first to use changes in carotid blood flow to assess fluid responsiveness. Because the CCA is a large, superficial, readily accessible artery, we reasoned that carotid Doppler flow imaging would be a simple, noninvasive method to assess volume responsiveness. We had a priori hypothesized that the percent increase in carotid blood flow would parallel the change in SVI. However, we noted that in hemodynamically unstable volume responders, there was a preferential distribution of blood toward the carotid circulation (and brain) and away from the peripheries (brachial circulation) following the fluid challenge. (SVI increased 29% after a PLR maneuver, yet the carotid blood flow increased 79% and the brachial blood flow increased 12%.) Physiologically, this makes sense because the blood vessels of the brain (as well as of the heart and kidney) are low-resistance vessels that will preferentially divert blood to these vital vascular beds during low perfusion states. It is noteworthy that these vessels receive a substantial proportion of blood flow during diastole, whereas there is no or reverse flow in high-resistance vessels during diastole (Figs 1, 2). The present findings are supported by classic studies performed in the 1960s and 1970s using labeled microspheres in monkeys and dogs exposed to hemorrhagic and endotoxic shock, which demonstrated preferential redistribution of blood to the brain, heart, and adrenal gland.2729 Carotid Doppler flow imaging provided us with a very simple method to confirm these findings. Furthermore, carotid Doppler flow studies may provide a simple, readily accessible, and sensitive site to monitor for changes in cerebral blood flow following a therapeutic intervention. We have previously noted that in healthy volunteers, PLR causes, on average, a 33% increase in SVI, whereas carotid blood flow increased by only 16% (P. E. Marik, MD, and A. Levitov, MD, RDCS, FCCP, unpublished data, May 2012). Additionally, with Sirsha-asana (yoga headstand), cerebral blood flow remains unchanged. These data suggest that the brain tightly regulates cerebral blood flow according to demand with a selective redistribution during low perfusion states. An additional implication of this work suggests that because of redistribution away from the peripheries (especially the brachial artery), the radial artery would be a very poor site to monitor for changes in stroke volume.30,31

An additional unexpected finding in the present study was a significant increase in the caliber of the CCA in the fluid responders. This phenomenon, known as flow-mediated dilation (FMD), is well known to vascular biologists and is used a marker of endothelial integrity. In 1992, Celermajer et al32 developed the FMD technique as a noninvasive method to measure vascular endothelial function. The ultrasonic assessment of FMD in response to occlusion-induced hyperemia has been established as a reliable, noninvasive measurement of endothelial function and has been documented to correlate with invasively assessed endothelial function in the coronary arteries.33 The assessment of endothelial function through FMD has been proposed to represent a functional bioassay for endothelium-derived nitric oxide (NO) bioavailability in humans.34,35 The increased flow increases laminar shear forces, which are transduced through luminal mechanoreceptors, resulting in increased expression of endothelial NO synthase activity, which catalyzes the conversion of L-arginine to NO.35 The significance of the FMD in the present study patients is unclear; however, it provides a new avenue to assessing endothelial function in hemodynamically unstable patients with sepsis.

In conclusion, we have demonstrated that a PLR maneuver coupled with the bioreactance noninvasive CO monitor is a simple and accurate method of assessing volume responsiveness in critically ill patients. In addition, the study suggests that changes in carotid blood flow following a PLR maneuver may be a useful adjunctive method for determining fluid responsiveness in hemodynamically unstable patients.

Author contributions: Dr Marik had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.

Dr Marik: contributed to the study design, data collection and analysis, writing of the manuscript, and review and final approval of the manuscript.

Dr Levitov: contributed to the study design, data collection, writing of the manuscript, and review and final approval of the manuscript.

Dr Young: contributed to the data collection, writing of the manuscript, and review and final approval of the manuscript.

Ms Andrews: contributed to the data collection, writing of the manuscript, and review and final approval of the manuscript.

Financial/nonfinancial disclosures: The authors have reported to CHEST the following conflicts of interest: Ms Andrews serves as an educator and clinical consultant for a company that sells invasive hemodynamic monitoring equipment. Drs Marik, Levitov, and Young have reported that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

CCA

common carotid artery

CO

cardiac output

FMD

flow-mediated dilation

LVEF

left ventricular ejection fraction

NO

nitric oxide

PLR

passive leg raising

SVI

stroke volume index

SVV

stroke volume variation

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Figures

Figure Jump LinkFigure 1. Carotid artery Doppler flow imaging at baseline and after a passive leg raising maneuver in a fluid responder. Carotid blood flow increased by 80%, and the vascular diameter increased by 20%. Note the increase in both systolic and diastolic flow. ED = end-diastolic velocity; PS = peak systolic velocity; TAMAX = time average maximum; TAMEAN = time average mean; VF = volume flow.Grahic Jump Location
Figure Jump LinkFigure 2. Brachial artery Doppler flow imaging at baseline and after a passive leg raising maneuver in a fluid responder. Brachial blood flow increased by 7%, and the vascular diameter remained unchanged. Note the absence of diastolic blood flow. See Figure 1 legend for expansion of abbreviations.Grahic Jump Location

Tables

Table Graphic Jump Location
Table 1 —PLR Responder and Nonresponder Characteristics

Data are presented as mean ± SD or counts. CO = cardiac output; PLR = passive leg raising; SVI = stroke volume index.

a 

Bilateral carotid blood flow as percentage of CO.

References

Shapiro NI, Howell MD, Talmor D, et al. Implementation and outcomes of the Multiple Urgent Sepsis Therapies (MUST) protocol. Crit Care Med. 2006;34(4):1025-1032. [CrossRef] [PubMed]
 
Jones AE, Shapiro NI, Trzeciak S, Arnold RC, Claremont HA, Kline JA; Emergency Medicine Shock Research Network (EMShockNet) Investigators Emergency Medicine Shock Research Network (EMShockNet) Investigators. Lactate clearance vs central venous oxygen saturation as goals of early sepsis therapy: a randomized clinical trial. JAMA. 2010;303(8):739-746. [CrossRef] [PubMed]
 
Jones AE, Brown MD, Trzeciak S, et al;; Emergency Medicine Shock Research Network investigators Emergency Medicine Shock Research Network investigators. The effect of a quantitative resuscitation strategy on mortality in patients with sepsis: a meta-analysis. Crit Care Med. 2008;36(10):2734-2739. [CrossRef] [PubMed]
 
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